This study seeks to validate an approach to cancer chemotherapy based on the interruption of cancer cachexia. Specifically, inhibition of gluconeogenesis at the phosphoenolpyruvate carboxykinase (PEP CK) level, representing an attack on the host's thermodynamic participation in the malignant process, is aimed at retarding host energy loss attendant upon augmented gluconeogenesis in the disease. Since host energy loss (cachexia) and tumor energy gain (tumor growth) appear to be functionally interrelated, a block to one may result in a block to the other; thus agents which interfere with gluconeogenesis in the host may also intefere with tumor growth itself. Experimental results to date confirm that PEP CK inhibitors produce in-vivo tumor inhibition in various transplantable animal tumors. Such experiments will be expanded as this study progresses. Emphasis will be placed on the concurrent exploration of biochemical mechanisms operative during the course of administration of gluconeogenic blocking agents. BIBLIOGRAPHIC REFERENCES: Gold, J.: Use of Hydrazine Sulfate in Terminal and Pre-terminal Cancer Patients: Preliminary Results of Pharmaceutical IND Study, Proc. Amer. Assn. Cancer Res. 16:9, 1975. Gold, J.: Enhancement by Hydrazine Sulfate of Antitumor Effectiveness of Cytoxan, Mitomycin C, Methotrexate and Bleomycin, in Walker 256 Carcinosarcoma in Rats, Oncology 31:44-53, 1975.